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高糖基化结合蛋白 17(FBP17)的表达表明导管癌分化不良和侵袭性强。

High formin binding protein 17 (FBP17) expression indicates poor differentiation and invasiveness of ductal carcinomas.

机构信息

Laboratory of Molecular Medicine, Department of Human Genetics and Molecular Medicine, Central University of Punjab, Bathinda, 151001, India.

Department of Vascular Cell Biology, Max Planck Institute for Molecular Biomedicine, 48149, Münster, Germany.

出版信息

Sci Rep. 2020 Jul 14;10(1):11543. doi: 10.1038/s41598-020-68454-9.

DOI:10.1038/s41598-020-68454-9
PMID:32665637
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7360568/
Abstract

Formin binding protein 17 (FBP17) belongs to Cdc-42 interacting protein 4 subfamily of F-BAR proteins. Recently, we had reported that FBP17 was overexpressed in invasive breast cancer cells and interacts with the actin regulatory proteins. We also reported that FBP17 promotes invadopodia formation and enhances extracellular matrix degradation. The current study determines FBP17 expression in invasive ductal carcinomas (IDCs) using breast cancer tissue microarrays (TMAs) (82 IDCs with variable receptor status and 8 Normal adjacent tissues) and its correlation with the clinico-pathological features. Immunohistochemistry of human breast cancer TMAs showed the significant elevation in the levels of FBP17 in breast cancer tissues than the normal (p ≤ 0.0001). Interestingly, FBP17 had a higher expression in invasive molecular subtypes HER2 and TNBC (p ≤ 0.05). Similarly, tumors with lymph node positive status showed elevated FBP17 expression in HER2 and TNBC subtypes (p ≤ 0.05). Surprisingly, grade 3 tumors demonstrated higher FBP17 expression (p ≤ 0.01) indicating its role in poorly differentiated tumors. Together, the data demonstrates the overexpression of FBP17 in invasive and poorly differentiated tumors. Understanding the role of FBP17 in poor differentiation and invasion of tumors in molecular subtypes at various level might represent as a potential molecular target against the disease.

摘要

formin 结合蛋白 17(FBP17)属于 Cdc-42 相互作用蛋白 4 亚家族的 F-BAR 蛋白。最近,我们报道称 FBP17 在浸润性乳腺癌细胞中过表达,并与肌动蛋白调节蛋白相互作用。我们还报道称,FBP17 促进侵袭伪足的形成并增强细胞外基质的降解。本研究使用乳腺癌组织微阵列(TMA)(82 例具有不同受体状态的浸润性导管癌和 8 例正常相邻组织)来确定 FBP17 在浸润性导管癌(IDC)中的表达及其与临床病理特征的相关性。人乳腺癌 TMA 的免疫组织化学显示,FBP17 在乳腺癌组织中的水平明显高于正常组织(p≤0.0001)。有趣的是,FBP17 在侵袭性分子亚型 HER2 和三阴性乳腺癌(TNBC)中的表达更高(p≤0.05)。同样,淋巴结阳性状态的肿瘤在 HER2 和 TNBC 亚型中显示出 FBP17 表达的升高(p≤0.05)。令人惊讶的是,3 级肿瘤表现出更高的 FBP17 表达(p≤0.01),表明其在分化不良的肿瘤中发挥作用。总之,数据表明 FBP17 在浸润性和分化不良的肿瘤中过度表达。了解 FBP17 在分子亚型中肿瘤低分化和侵袭的作用可能代表着针对该疾病的潜在分子靶标。

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